Frontiers in Neuroscience,
Journal Year:
2023,
Volume and Issue:
17
Published: March 14, 2023
Spinal
cord
injury
is
a
serious
traumatic
disease.
As
Ferroptosis
has
been
increasingly
studied
in
recent
years,
it
found
to
be
closely
related
the
pathophysiological
processes
of
spinal
injury.
Iron
overload,
reactive
oxygen
species
accumulation,
lipid
peroxidation
and
glutamate
accumulation
associated
with
are
all
present
injury,
thus
thought
involved
pathological
secondary
This
article
highlights
relationship
between
lists
substances
that
improve
by
inhibiting
Ferroptosis,
concludes
discussion
problems
may
encountered
clinical
translation
inhibitors
as
means
enabling
their
faster
use
treatment.
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: Dec. 10, 2023
Abstract
Ferroptosis,
a
unique
modality
of
cell
death
with
mechanistic
and
morphological
differences
from
other
modes,
plays
pivotal
role
in
regulating
tumorigenesis
offers
new
opportunity
for
modulating
anticancer
drug
resistance.
Aberrant
epigenetic
modifications
posttranslational
(PTMs)
promote
resistance,
cancer
progression,
metastasis.
Accumulating
studies
indicate
that
can
transcriptionally
translationally
determine
vulnerability
to
ferroptosis
functions
as
driver
nervous
system
diseases
(NSDs),
cardiovascular
(CVDs),
liver
diseases,
lung
kidney
diseases.
In
this
review,
we
first
summarize
the
core
molecular
mechanisms
ferroptosis.
Then,
roles
processes,
including
histone
PTMs,
DNA
methylation,
noncoding
RNA
regulation
such
phosphorylation,
ubiquitination,
SUMOylation,
acetylation,
ADP-ribosylation,
are
concisely
discussed.
The
PTMs
genesis
cancers,
NSD,
CVDs,
well
application
PTM
modulators
therapy
these
then
discussed
detail.
Elucidating
mediated
by
will
facilitate
development
promising
combination
therapeutic
regimens
containing
or
PTM-targeting
agents
inducers
be
used
overcome
chemotherapeutic
resistance
could
prevent
addition,
highlight
potential
approaches
chemoresistance
halt
Experimental & Molecular Medicine,
Journal Year:
2023,
Volume and Issue:
55(8), P. 1620 - 1631
Published: Aug. 23, 2023
Abstract
Ferroptosis
is
a
form
of
regulated
cell
death
characterized
by
iron-dependent
lipid
peroxidation.
This
process
contributes
to
cellular
and
tissue
damage
in
various
human
diseases,
such
as
cardiovascular
neurodegeneration,
liver
disease,
cancer.
Although
polyunsaturated
fatty
acids
(PUFAs)
membrane
phospholipids
are
preferentially
oxidized,
saturated/monounsaturated
(SFAs/MUFAs)
also
influence
peroxidation
ferroptosis.
In
this
review,
we
first
explain
how
cells
differentially
synthesize
SFA/MUFAs
PUFAs
they
control
acid
pools
via
uptake
β-oxidation,
impacting
Furthermore,
discuss
stored
different
lipids,
diacyl
or
ether
with
head
groups;
triglycerides;
cholesterols.
Moreover,
these
released
from
molecules.
summary,
provide
an
integrated
view
the
diverse
dynamic
metabolic
processes
context
ferroptosis
revisiting
lipidomic
studies.
Thus,
review
development
therapeutic
strategies
for
ferroptosis-related
diseases.
Free Radical Biology and Medicine,
Journal Year:
2023,
Volume and Issue:
208, P. 348 - 360
Published: Aug. 26, 2023
Ferroptosis
in
tubules
has
been
implicated
the
pathogenesis
of
acute
kidney
injury
(AKI),
whereas
regulatory
mechanism
remains
unclear.
The
stimulator
interferon
genes
(STING)
is
previously
recognized
as
a
critical
mediator
innate
immunity
via
DNA-sensing
pathway
and
increasingly
linked
to
lipid
peroxidation,
hallmark
ferroptosis.
Herein
we
investigated
role
underlying
STING
AKI
models
established
by
ischemia/reperfusion
(IR)
C57BL
mice.
expression
level
was
predominantly
increased
after
IR
treatment.
Besides,
deficiency
markedly
alleviated
IR-induced
tissue
damage
renal
dysfunction.
Consistently,
vitro
experiments
demonstrated
that
increase
ferroptotic
cell
death,
ROS
production
decrease
GSH
peroxidase
4
(GPX4)
tubular
cells
subjected
ferroptosis
agonist
or
hypoxia/reoxygenation
intervention
were
all
mitigated
genetic
pharmacological
inhibition
STING,
while
exacerbated
overexpression.
Further,
these
detrimental
effects
overexpression
relied
on
induction
ferritinophagy,
i.e.
autophagic
degradation
ferritin,
leading
iron
overload.
Mechanistically,
mediated
initiation
ferritinophagy
through
interacting
with
nuclear
receptor
coactivator
(NCOA4),
fundamental
for
transfer
ferritin
into
lysosome.
Collectively,
contributes
during
ischemic
facilitating
NCOA4-mediated
shows
potential
promising
therapeutic
choice
AKI.
Cell Death Discovery,
Journal Year:
2024,
Volume and Issue:
10(1)
Published: May 4, 2024
Abstract
Renal
ischemia‒reperfusion
injury
(IRI)
is
one
of
the
main
causes
acute
kidney
(AKI),
which
a
potentially
life-threatening
condition
with
high
mortality
rate.
IRI
complex
process
involving
multiple
underlying
mechanisms
and
pathways
cell
dysfunction.
Additionally,
various
types
death
have
been
linked
to
IRI,
including
necroptosis,
apoptosis,
pyroptosis,
ferroptosis.
These
processes
operate
differently
varying
degrees
in
different
patients,
but
each
plays
role
pathological
conditions
AKI.
Advances
understanding
pathophysiology
will
lead
development
new
therapeutic
approaches
that
hold
promise
for
improving
outcomes
patients
This
review
provides
an
overview
recent
research
on
molecular
IRI-AKI,
focus
regulated
(RCD)
forms
such
as
Overall,
targeting
RCD
shows
potential
approach
treating
IRI-AKI.
Advanced Healthcare Materials,
Journal Year:
2023,
Volume and Issue:
12(12)
Published: Jan. 19, 2023
Ferroptosis
is
a
non-apoptotic
programmed
cell
death
caused
by
the
accumulation
of
lipid
peroxide.
System
Xc-/glutathione
peroxidase
4
(GPX4)
axis
and
iron
are
two
main
pathways
regulating
ferroptosis.
Simultaneously,
multiple
also
involved
in
ferroptosis
regulation.
an
intense
area
current
study.
With
improvement
regulatory
mechanisms
that
underlie
ferroptosis,
variety
drugs
associated
with
have
been
discovered
developed
for
cancer
therapy.
Among
them,
traditional
were
initially.
Small
molecule
compounds
regulate
signaling
pathway
complexes
promote
Fenton
reaction
become
important
inducing
In
recent
years,
emerging
development
nanotechnology
has
promoted
research
nanodrugs.
Iron-based
nanomaterials
extensively
tested
as
ferroptosis-inducing
agents.
Furthermore,
nanoscale
drug
delivery
systems
offer
suitable
scaffold
therapies.
Traditional
nanodrugs
complementary,
each
their
own
strengths
limitations.
This
review
describes
latest
studies
on
regulation
tumor
cells
focuses
entanglement
between
To
conclude,
challenges
perspectives
this
field
put
forward.
International Journal of Biological Sciences,
Journal Year:
2023,
Volume and Issue:
19(12), P. 3726 - 3743
Published: Jan. 1, 2023
Ferroptosis
is
an
iron-dependent
programmed
cell
death
pattern
that
characterized
by
iron
overload,
reactive
oxygen
species
(ROS)
accumulation
and
lipid
peroxidation.
Growing
viewpoints
support
the
imbalance
of
homeostasis
disturbance
metabolism
contribute
to
tissue
or
organ
injury
in
various
kidney
diseases
triggering
ferroptosis.
At
present,
key
regulators
complicated
network
mechanisms
associated
with
ferroptosis
have
been
deeply
studied;
however,
its
role
initiation
progression
has
not
fully
revealed.
Herein,
we
aim
discuss
features,
ferroptosis,
explore
emerging
roles
organelles
gather
pharmacological
progress,
systematically
summarize
most
recent
discoveries
about
crosstalk
between
diseases,
including
renal
carcinoma
(RCC),
acute
(AKI),
diabetic
disease
(DKD),
autosomal
dominant
polycystic
(ADPKD),
fibrosis,
lupus
nephritis
(LN)
IgA
nephropathy.
We
further
conclude
potential
therapeutic
strategies
targeting
for
prevention
treatment
hope
this
work
will
provide
insight
study
pathogenesis
kidney-related
diseases.
Molecular Medicine,
Journal Year:
2023,
Volume and Issue:
29(1)
Published: April 3, 2023
Abstract
Background
Ferroptosis,
which
is
characterized
by
lipid
peroxidation
and
iron
accumulation,
closely
associated
with
the
pathogenesis
of
acute
renal
injury
(AKI).
Cyanidin-3-glucoside
(C3G),
a
typical
flavonoid
that
has
anti-inflammatory
antioxidant
effects
on
ischemia‒reperfusion
(I/R)
injury,
can
induce
AMP-activated
protein
kinase
(AMPK)
activation.
This
study
aimed
to
show
C3G
exerts
nephroprotective
against
I/R-AKI
related
ferroptosis
regulating
AMPK
pathway.
Methods
Hypoxia/reoxygenation
(H/R)-induced
HK-2
cells
mice
were
treated
or
without
inhibiting
AMPK.
The
level
intracellular
free
iron,
expression
ferroptosis-related
proteins
acyl-CoA
synthetase
long
chain
family
member
4
(ACSL4)
glutathione
peroxidase
(GPX4),
levels
markers
4-hydroxynonenal
(4-HNE),
reactive
oxygen
species
(ROS)
malondialdehyde
(MDA)
examined.
Results
We
observed
inhibitory
effect
in
vitro
vivo,
was
reversion
excessive
decrease
4-HNE,
ROS,
MDA
ACSL4
expression,
an
increase
GPX4
(GSH)
levels.
Notably,
inhibition
CC
significantly
abrogated
models
vivo
vitro.
Conclusion
Our
results
provide
new
insight
into
activating